Abstract
The lymphatic system is involved in pathogenesis of edema, inflammation and cancer metastasis. It has been reported that lymph capillary network regulates interstitial electrolyte and volume balance, which buffers blood pressure. Thus, we hypothesized that impaired lymphatics dysfunction leads to increasing blood pressure. In this study, we employed thoracic duct from 10-14-week-old Wister-Kyoto (WKY) and spontaneously hypertensive rats (SHR) and examined lymphatics contractility. Thoracic duct from SHR exhibited impaired acetylcholine (ACh)-induced endothelial-dependent relaxation compared to age-matched WKY (39.4±1.0% vs 84.8±2.2%, p<0.05). L-NAME, a NOS inhibitor blunted ACh-induced relaxation in WKY and SHR. Tempol, a superoxide dismutase mimetic significantly improved the impairment in SHR (p<0.05). Thoracic duct from SHR also displayed decreased SNP-induced relaxation (p<0.05). Despite the marked impairment in relaxation, contraction response to angiotensin II in SHR was similar to WKY. We conclude that lymphatic function was significantly blunted in hypertensive model at least SHR through superoxide. The impairment of the lymphatic relaxation may be involved in increased blood pressure in hypertension due to dysfunction of lymphatic buffering.
